Living high training low induces physiological cardiac hypertrophy accompanied by down-regulation and redistribution of the renin-angiotensin system

Abstract

Aim:

Living high training low” (LHTL) is an exercise-training protocol that refers living in hypoxia stress and training at normal level of O ₂. In this study, we investigated whether LHTL caused physiological heart hypertrophy accompanied by changes of biomarkers in renin-angiotensin system in rats.

Methods:

Adult male SD rats were randomly assigned into 4 groups, and trained on living low-sedentary (LLS, control), living low-training low (LLTL), living high-sedentary (LHS) and living high-training low (LHTL) protocols, respectively, for 4 weeks. Hematological parameters, hemodynamic measurement, heart hypertrophy and plasma angiotensin II (Ang II) level of the rats were measured. The gene and protein expression of angiotensin-converting enzyme (ACE), angiotensinogen (AGT) and angiotensin II receptor I (AT ₁) in heart tissue was assessed using RT-PCR and immunohistochemistry, respectively.

Results:

LLTL, LHS and LHTL significantly improved cardiac function, increased hemoglobin concentration and RBC. At the molecular level, LLTL, LHS and LHTL significantly decreased the expression of ACE, AGT and AT ₁ genes, but increased the expression of ACE and AT ₁ proteins in heart tissue. Moreover, ACE and AT ₁ protein expression was significantly increased in the endocardium, but unchanged in the epicardium.

Conclusion:

LHTL training protocol suppresses ACE, AGT and AT1 gene expression in heart tissue, but increases ACE and AT ₁ protein expression specifically in the endocardium, suggesting that the physiological heart hypertrophy induced by LHTL is regulated by region-specific expression of renin-angiotensin system components.